Neurotrophic action of lipocortin 1 derived from astrocytes on cultured rat cortical neurons

Mizuno, Haruo; Asai, Kiyofumi; Fujita, Kaori; Uemura, Kenji; Wada, Yoshiro; Moriyama, Akihiko; Ogawa, Hidenori; Kimura, Shigeki; Kato, Taiji

doi:10.1016/s0169-328x(98)00163-6

Cited by 12 publications

(11 citation statements)

References 34 publications

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“…We found that Dex induced the expression of NT-3 mRNA in cultured astrocytes. We reported previously that Dex induces lipocortin-1 mRNA in astrocytes and that lipocortin-1 has a neurotrophic effect on cultured cortical neurons (24). These data suggest that glucocorticoid induced by ACTH 1-24 may also have neurotrophic effects by inducing NT-3 and lipocortin-1 in astrocytes.…”

Section: Discussionmentioning

confidence: 62%

ACTH1–24 Down-Regulates Expression of Ciliary Neurotrophic Factor mRNA in Cultured Rat Astrocyte

et al. 2002

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We examined the effects on astrocytes of ACTH, which is used to treat West syndrome. We stimulated cultured rat astrocytes with ACTH 1-24 , corticotropin-releasing factor, and dexamethasone, and examined changes in neurotrophic factor mRNAs by reverse transcription-PCR. Downregulation of ciliary neurotrophic factor mRNA expression was observed by stimulation with ACTH 1-24 , but the expression of nerve growth factor, brain-derived neurotrophic factor, and nerotrophin-3 mRNAs was unaffected. Northern blot analysis revealed that the decrease in ciliary neurotrophic factor mRNA occurred 4 h after stimulation with more than 10 nM of ACTH 1-24 . Up-regulation of nerotrophin-3 mRNA expression was found after stimulation with 1 mM dexamethasone. These results suggest that ACTH ACTH is a 39-amino acid peptide that is derived from the precursor peptide pro-opiomelanocortin. Hypothalamic neurons contain most of the brain pro-opiomelanocortin-related peptides, but ACTH is also found in the amygdala, cerebral cortex, brainstem, and cerebellum (1). In addition to its classic function, ACTH is thought to act as a neurotransmitter, neuromodulator, and growth factor (1). ACTH has been demonstrated to have a neurotrophic effect, enhancing recovery from damage in both the peripheral nervous system and the CNS (2).West syndrome is an intractable epileptic encephalopathy in infants. The seizures are lessened by ACTH and glucocorticoids, both major components of the brain-adrenal axis (3), but ACTH is reported to be more effective than glucocorticoids (4, 5). However, the mechanism of action of ACTH on immature damaged brain, which may lead to West syndrome, has not been thoroughly investigated. ACTH and adrenal steroids may be important regulators of trophic processes operative in synaptic plasticity (6). It has been reported that not only neurons but also astrocytes express ACTH-receptors and that ACTH induces morphologic changes in astrocytes (7). Thus, ACTH 1-24 administrated in West syndrome may have some influence on astrocytes in vivo. Astrocytes express several kinds of neurotrophic factors and extracellular matrices that regulate axonal growth or regeneration after injury. In view of the therapy for West syndrome, it might be important to examine the influence of ACTH on astrocytes, especially with respect to the expression of neurotrophic factors. 0031-3998/02/5206-0950 PEDIATRIC RESEARCH Vol. 52, No. 6, 2002 Copyright © 2002 Printed in U.S.A. METHODS ABSTRACT950

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Section: Discussionmentioning

confidence: 62%

ACTH1–24 Down-Regulates Expression of Ciliary Neurotrophic Factor mRNA in Cultured Rat Astrocyte

et al. 2002

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“…Annexins I and V were also found to have neurotrophic effects on cultured neurons [44, 45]. Han et al [46] studied the effects of the annexins II and V on the survival of neurons and astrocytes in vitro .…”

Section: Discussionmentioning

confidence: 99%

The Proteome of the Differentiating Mesencephalic Progenitor Cell Line CSM14.1In Vitro

Weiß

Haas

Lessner

et al. 2014

BioMed Research International

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The treatment of Parkinson's disease by transplantation of dopaminergic (DA) neurons from human embryonic mesencephalic tissue is a promising approach. However, the origin of these cells causes major problems: availability and standardization of the graft. Therefore, the generation of unlimited numbers of DA neurons from various types of stem or progenitor cells has been brought into focus. A source for DA neurons might be conditionally immortalized progenitor cells. The temperature-sensitive immortalized cell line CSM14.1 derived from the mesencephalon of an embryonic rat has been used successfully for transplantation experiments. This cell line was analyzed by unbiased stereology of cell type specific marker proteins and 2D-gel electrophoresis followed by mass spectrometry to characterize the differentially expressed proteome. Undifferentiated CSM14.1 cells only expressed the stem cell marker nestin, whereas differentiated cells expressed GFAP or NeuN and tyrosine hydroxylase. An increase of the latter cells during differentiation could be shown. By using proteomics an explanation on the protein level was found for the observed changes in cell morphology during differentiation, when CSM14.1 cells possessed the morphology of multipolar neurons. The results obtained in this study confirm the suitability of CSM14.1 cells as an in vitro model for the study of neuronal and dopaminergic differentiation in rats.

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“…Previous studies showed that the expression of annexins I, II, V increased in the spinal cord tissue adjacent to the transection [13] or the contusion [14] region, and it is believed that these annexins exert anti-inflammatory actions through the inhibition of PLA 2 activity [5,15] , a key enzyme responsible for inflammation and cytotoxicity [16][17] . An anti-inflammatory effect of annexin I was confirmed in vitro; furthermore, neurotrophic effects of annexins I and V on cultured neurons were also revealed [18][19][20] ; however, the effects of annexin II on posttraumatic insults remain unclear.…”

Section: Introductionmentioning

confidence: 93%

Anti-Neuroinflammatory and Neurotrophic Effects of Combined Therapy with Annexin II and Reg-2 on Injured Spinal Cord

Fang

Huang²,

Wang³

et al. 2011

Neurosignals

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The present study was designed to investigate the neuroprotective effects of Ca²⁺-dependent phospholipid-binding protein annexin II and a secreted protein Reg-2 (regeneration gene protein 2) in spinal cord injury (SCI) model produced by contusion SCI at T₉ using the weight drop method. The agents were delivered intrathecally with Alzet miniosmotic pumps. We found that annexin II and Reg-2 remarkably reduced neuronal death, attenuated tissue damage and alleviated detrimental inflammation in vivo; meanwhile, a significant increase in white matter sparing and myelination area was observed. The propriospinal axons and long-distance supraspinal pathways were protected by the treatments as revealed by retrograde tracing. Basso Beattie Bresnahan locomotor rating scores also revealed a measurable behavioral improvement. However, no evident behavioral improvements in locomotor performance were achieved by the combined treatment with annexin II and Reg-2, compared with the separate treatment with annexin II and Reg-2.

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Neurotrophic action of lipocortin 1 derived from astrocytes on cultured rat cortical neurons

Cited by 12 publications

References 34 publications

ACTH1–24 Down-Regulates Expression of Ciliary Neurotrophic Factor mRNA in Cultured Rat Astrocyte

ACTH1–24 Down-Regulates Expression of Ciliary Neurotrophic Factor mRNA in Cultured Rat Astrocyte

The Proteome of the Differentiating Mesencephalic Progenitor Cell Line CSM14.1In Vitro

Anti-Neuroinflammatory and Neurotrophic Effects of Combined Therapy with Annexin II and Reg-2 on Injured Spinal Cord

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